ArticleScientific reports2016
Analysis of Post-Traumatic Brain Injury Gene Expression Signature Reveals Tubulins, Nfe2l2, Nfkb, Cd44, and S100a4 as Treatment Targets.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Pooled it
- CSF1R and IL1R1 inhibitors synergistically attenuate the early pathogenesis of traumatic brain injury in mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Elastin-like polypeptide delivery of an NF-kB inhibitor for treatment of juvenile mild TBI complicated by high-fat diet consumption.Experimental neurology · 2025Article
- Cyclosporine A Accelerates Neurorecovery Transcriptional Trajectory in a Swine Model of Diffuse Traumatic Brain Injury.International journal of molecular sciences · 2025Article
- Role of damage-associated molecular patterns in the pathogenesis and therapeutics of traumatic brain injury.Burns & trauma · 2025Review
- Identification and Validation of Endoplasmic Reticulum Stress-Related Gene in Traumatic Brain Injury.Journal of molecular neuroscience : MN · 2024Article
- Identification of potential crucial genes and therapeutic targets for epilepsy.European journal of medical research · 2024Article
- Treatment of Status Epilepticus after Traumatic Brain Injury Using an Antiseizure Drug Combined with a Tissue Recovery Enhancer Revealed by Systems Biology.International journal of molecular sciences · 2023Article
- Article
- Understanding microglial responses in large animal models of traumatic brain injury: an underutilized resource for preclinical and translational research.Journal of neuroinflammation · 2023Review
- Gene Expression Profile as a Predictor of Seizure Liability.International journal of molecular sciences · 2023Article
- Tandem Mass Tag-based proteomics analysis reveals the vital role of inflammation in traumatic brain injury in a mouse model.Neural regeneration research · 2023Article
- Alterations of microRNAs expression profiles in small extracellular vesicle after traumatic brain injury in mice.Experimental animals · 2022Article
- Comprehensive RNA Expression Analysis Revealed Biological Functions of Key Gene Sets and Identified Disease-Associated Cell Types Involved in Rat Traumatic Brain Injury.Journal of clinical medicine · 2022Article
- Transfer RNA-Derived Fragments and isomiRs Are Novel Components of Chronic TBI-Induced Neuropathology.Biomedicines · 2022Article
- Transcriptional Profiling in a Novel Swine Model of Traumatic Brain Injury.Neurotrauma reports · 2022Article
- Glial immune-related pathways mediate effects of closed head traumatic brain injury on behavior and lethality in Drosophila.PLoS biology · 2022Article
- Drug connectivity mapping and functional analysis reveal therapeutic small molecules that differentially modulate myelination.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Article
- Real-Time Noninvasive Bioluminescence, Ultrasound and Photoacoustic Imaging in NFκB-RE-Luc Transgenic Mice Reveal Glia Maturation Factor-Mediated Immediate and Sustained Spatio-Temporal Activation of NFκB Signaling Post-Traumatic Brain Injury in a Gender-Specific Manner.Cellular and molecular neurobiology · 2021Article
- Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We aimed to define the chronically altered gene expression signature of traumatic brain injury (TBI-sig) to discover novel treatments to reverse pathologic gene expression or reinforce the expression of recovery-related genes. Genome-wide RNA-sequencing was performed at 3 months post-TBI induced by lateral fluid-percussion injury in rats. We found 4964 regulated genes in the perilesional cortex and 1966 in the thalamus (FDR < 0.05). TBI-sig was used for a LINCS analysis which identified 11 compounds that showed a strong connectivity with the TBI-sig in neuronal cell lines. Of these, celecoxib and sirolimus were recently reported to have a disease-modifying effect in in vivo animal models of epilepsy. Other compounds revealed by the analysis were BRD-K91844626, BRD-A11009626, NO-ASA, BRD-K55260239, SDZ-NKT-343, STK-661558, BRD-K75971499, ionomycin, and desmethylclomipramine. Network analysis of overlapping genes revealed the effects on tubulins (Tubb2a, Tubb3, Tubb4b), Nfe2l2, S100a4, Cd44, and Nfkb2, all of which are linked to TBI-relevant outcomes, including epileptogenesis and tissue repair. Desmethylclomipramine modulated most of the gene targets considered favorable for TBI outcome. Our data demonstrate long-lasting transcriptomics changes after TBI. LINCS analysis predicted that these changes could be modulated by various compounds, some of which are already in clinical use but never tested in TBI.
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